Damage of the glomerular filtration barrier leads to proteinuria and progressive renal failure. Several independent lines of research have implicated the glomerular epithelial cell (GEC) as a key player in initiation and propagation of pathways leading to glomerulosclerosis. A growing number of molecules activated in this process have been identified. To further define their cellular function, manipulation of these molecules using pharmacological or genetic approaches in tissue culture systems are required. In this study, strategies for altering GEC gene expression by transient and stable transfection of fluorescence labeled proteins will be presented and discussed. The insight gained through these and comparable systems should allow a detailed dissection of the molecular pathways active in GEC function and failure.